Nitroglycerin-induced headache is not dependent on histamine release: support for a direct nociceptive action of nitric oxide

Helle Klingenberg Iversen; J Olesen

Nitroglycerin-induced headache is not dependent on histamine release: support for a direct nociceptive action of nitric oxide

Institut for Klinisk Medicin

42 Citationer (Scopus)

Abstract

The molecular mechanisms of migraine pain have not yet been clarified. Monoamine and the peptide neurotransmitters involved in neurogenic inflammation do not cause significant head pain. Our previous studies of glyceryl trinitrate (GTN) and histamine-induced headaches have suggested that nitric oxide (NO) is the causative molecule in migraine pain. We furthermore suggest that substances capable of inducing experimental vascular headache do so via a common mediator which is NO. Finally, it is suggested that drugs exert their antimigraine activity by inhibiting NO or subsequent steps in the cascade of intracellular reactions triggered by NO. These novel observations change current views on vascular headache mechanisms and the importance of NO as an initiator of the migraine attacks dictates new approaches to the pharmacological treatment of migraine and other vascular headaches.

Originalsprog	Engelsk
Tidsskrift	Cephalalgia : an international journal of headache
Vol/bind	14
Udgave nummer	6
Sider (fra-til)	437-42
Antal sider	6
ISSN	0333-1024
Status	Udgivet - dec. 1994

Citationsformater

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title = "Nitroglycerin-induced headache is not dependent on histamine release: support for a direct nociceptive action of nitric oxide",

abstract = "The molecular mechanisms of migraine pain have not yet been clarified. Monoamine and the peptide neurotransmitters involved in neurogenic inflammation do not cause significant head pain. Our previous studies of glyceryl trinitrate (GTN) and histamine-induced headaches have suggested that nitric oxide (NO) is the causative molecule in migraine pain. We furthermore suggest that substances capable of inducing experimental vascular headache do so via a common mediator which is NO. Finally, it is suggested that drugs exert their antimigraine activity by inhibiting NO or subsequent steps in the cascade of intracellular reactions triggered by NO. These novel observations change current views on vascular headache mechanisms and the importance of NO as an initiator of the migraine attacks dictates new approaches to the pharmacological treatment of migraine and other vascular headaches.",

keywords = "Analysis of Variance, Cross-Over Studies, Double-Blind Method, Headache, Hemodynamics, Histamine Release, Humans, Nitric Oxide, Nitroglycerin, Pain, Radial Artery, Reproducibility of Results, Temporal Arteries",

author = "Iversen, {Helle Klingenberg} and J Olesen",

year = "1994",

month = dec,

language = "English",

volume = "14",

pages = "437--42",

journal = "Cephalalgia, Supplement",

issn = "0800-1952",

publisher = "SAGE Publications",

number = "6",

}

TY - JOUR

T1 - Nitroglycerin-induced headache is not dependent on histamine release

T2 - support for a direct nociceptive action of nitric oxide

AU - Iversen, Helle Klingenberg

AU - Olesen, J

PY - 1994/12

Y1 - 1994/12

N2 - The molecular mechanisms of migraine pain have not yet been clarified. Monoamine and the peptide neurotransmitters involved in neurogenic inflammation do not cause significant head pain. Our previous studies of glyceryl trinitrate (GTN) and histamine-induced headaches have suggested that nitric oxide (NO) is the causative molecule in migraine pain. We furthermore suggest that substances capable of inducing experimental vascular headache do so via a common mediator which is NO. Finally, it is suggested that drugs exert their antimigraine activity by inhibiting NO or subsequent steps in the cascade of intracellular reactions triggered by NO. These novel observations change current views on vascular headache mechanisms and the importance of NO as an initiator of the migraine attacks dictates new approaches to the pharmacological treatment of migraine and other vascular headaches.

AB - The molecular mechanisms of migraine pain have not yet been clarified. Monoamine and the peptide neurotransmitters involved in neurogenic inflammation do not cause significant head pain. Our previous studies of glyceryl trinitrate (GTN) and histamine-induced headaches have suggested that nitric oxide (NO) is the causative molecule in migraine pain. We furthermore suggest that substances capable of inducing experimental vascular headache do so via a common mediator which is NO. Finally, it is suggested that drugs exert their antimigraine activity by inhibiting NO or subsequent steps in the cascade of intracellular reactions triggered by NO. These novel observations change current views on vascular headache mechanisms and the importance of NO as an initiator of the migraine attacks dictates new approaches to the pharmacological treatment of migraine and other vascular headaches.

KW - Analysis of Variance

KW - Cross-Over Studies

KW - Double-Blind Method

KW - Headache

KW - Hemodynamics

KW - Histamine Release

KW - Humans

KW - Nitric Oxide

KW - Nitroglycerin

KW - Pain

KW - Radial Artery

KW - Reproducibility of Results

KW - Temporal Arteries

M3 - Journal article

C2 - 7535192

SN - 0800-1952

VL - 14

SP - 437

EP - 442

JO - Cephalalgia, Supplement

JF - Cephalalgia, Supplement

IS - 6

ER -

Nitroglycerin-induced headache is not dependent on histamine release: support for a direct nociceptive action of nitric oxide

Abstract

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